Angiotensin II enhances responses to endothelin-1 in bovine bronchial smooth muscle
| Autor: | Jane E. Nally, Neil C. Thomson, John C. McGrath, R.A. Clayton, Michael J.O. Wakelam |
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| Rok vydání: | 1994 |
| Předmět: |
Pulmonary and Respiratory Medicine
Agonist medicine.medical_specialty Angiotensin receptor Indoles medicine.drug_class Tetrazoles Bronchi In Vitro Techniques Losartan Angiotensin Receptor Antagonists Internal medicine medicine Animals Pharmacology (medical) General Pharmacology Toxicology and Pharmaceutics Receptor Antihypertensive Agents Angiotensin II receptor type 1 Receptors Angiotensin biology Chemistry Receptors Endothelin Angiotensin II Endothelins Biphenyl Compounds Imidazoles Angiotensin-converting enzyme Drug Synergism Muscle Smooth Azepines Receptor antagonist Endocrinology cardiovascular system biology.protein Cattle medicine.drug Muscle Contraction |
| Zdroj: | Pulmonary pharmacology. 7(6) |
| ISSN: | 0952-0600 |
| Popis: | Summary: Angiotensin II and endothelin-1 are putative mediators in asthma. In this study we have examined the effect of angiotensin II on endothelin-1-induced contractions in bovine bronchi and the receptor types involved in the response to these agonists. Angiotensin II alone is very low in potency, producing only small contractions. In the presence of angiotensin II 10 -7 or 3 × 10 -7 M, contractions evoked by endothelin-1 were markedly enhanced. The AII 1 -receptor antagonist, losartan, abolished this enhancement suggesting that angiotensin II exerts this effect via an AII 1 -receptor. The contraction evoked by endothelin-1 is mediated via an Et A -receptor subtype since the Et A -receptor antagonist FR139317 attenuated the response. This is offset by an inhibitory Et B -type receptor, resulting in a larger contraction when these receptors are desensitized. Indeed, the Et B -receptor agonist sarafotoxin S6c reversed methacholine-evoked tone in a concentration-dependent manner. In conclusion, angiotensin II potentiates contractions evoked by endothelin-1 in bovine bronchi. This may be a mechanism by which angiotensin II—which has little activity in bronchi—may evoke substantial changes in airway tone. Angiotensin II evokes this potentiation via AII 1 -receptors, whilst endothelin-1 evokes contraction via Et A -receptors, an action which is offset by an inhibitory effect of Et B -receptors. |
| Databáze: | OpenAIRE |
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